Experimental study on the uptake and effects of arsenic originated from poultry litter on the growth of Brassica napus in greenhouse pot cultivation and health risk assessment

Organoarsenics are widely used as growth promoters in poultry industry,resulting in arsenic(As)accumulation in poultry litter.A greenhouse pot study was implemented to investigate the fate of arsenic originated from poultry litter and their effects on the growth of Brassica napus(oilseed rape),and assess their potential health risks.Five poultry litter application rates(0,5%,10%,20%and 40%)were used,dividing into two groups:one for soil incubation(SI)and the other for plant cultivation(PC).Experimental results indicated that the total arsenic for composted poultry litter was(10.94±0.23)mg/kg,As(V)and As(III)decreased while methylated arsenic increased after 21 d in SI and PC treatments.Seed germination rates were negatively correlated with monomethylarsenic acid(MMA,R2=0.63,p<0.05).The length and biomass of roots and shoots were significantly inhibited by poultry litter,but plant length of 5%treatments was slightly stimulated.Within an average weekly intake of 0.5 kg Brassica napuss,the risk quotient(RQ)values induced from roots nearly all surpassed the acceptable limit(1),were two orders magnitude higher than shoots.According to the potential risk to order,child exhibited the highest risk,adolescent ranked secondly,and adult exhibited the lowest risk.Hence,people should better avoid intake Brassica napus roots to reduce arsenic potential risk.

Arsenite provides a selective signal that coordinates arsenate uptake and detoxification through the regulation of PHR1 stability in Arabidopsis

In nature,plants acquire nutrients from soils to sustain growth,and at the same time,they need to avoid the uptake of toxic compounds and/or possess tolerance systems to cope with them.This is particularly challenging when the toxic compound and the nutrient are chemically similar,as in the case of phosphate and arsenate.In this study,we demonstrated that regulatory elements of the phosphate starvation response(PSR)coordinate the arsenate detoxification machinery in the cell.We showed that arsenate repression of the phosphate transporter PHT1;1 is associated with the degradation of the PSR master regulator PHR1.Once arsenic is sequestered into the vacuole,PHR1 stability is restored and PHT1;1 expression is recovered.Furthermore,we identified an arsenite responsive SKP1-like protein and a PHR1 interactor F-box(PHIF1)as constituents of the SCF complex responsible for PHR1 degradation.We found that arsenite,the form to which arsenate is reduced for compartmentalization in vacuoles,represses PHT1;1 expression,providing a highly selective signal versus phosphate to control PHT1;1 expression in response to arsenate.Collectively,our results provide molecular insights into a sensing mechanism that regulates arsenate/phosphate uptake depending on the plant’s detoxification capacity.

Cellular arsenic transport pathways in mammals

Natural contamination of drinking water with arsenic results in the exposure of millions of people world-wide to unacceptable levels of this metalloid. This is a serious global health problem because arsenic is a Group 1（proven） human carcinogen and chronic exposure is known to cause skin, lung, and bladder tumors. Furthermore, arsenic exposure can result in a myriad of other adverse health effects including diseases of the cardiovascular,respiratory, neurological, reproductive, and endocrine systems. In addition to chronic environmental exposure to arsenic, arsenic trioxide is approved for the clinical treatment of acute promyelocytic leukemia, and is in clinical trials for other hematological malignancies as well as solid tumors. Considerable inter-individual variability in susceptibility to arsenic-induced disease and toxicity exists, and the reasons for such differences are incompletely understood. Transport pathways that influence the cellular uptake and export of arsenic contribute to regulating its cellular, tissue, and ultimately body levels. In the current review, membrane proteins（including phosphate transporters, aquaglyceroporin channels, solute carrier proteins, and ATP-binding cassette transporters） shown experimentally to contribute to the passage of inorganic, methylated, and/or glutathionylated arsenic species across cellular membranes are discussed. Furthermore, what is known about arsenic transporters in organs involved in absorption, distribution, and metabolism and how transport pathways contribute to arsenic elimination are described.